The goal of this research is to study some of the mechanical factors affecting the normal physiology of pleural liquid exchange and their relationship to lung static recoil. Classical studies have postulated that pleural liquid pressure is less than pleural surface pressure (lung static recoil) and that pleural liquid is in hydrostatic equilibrium (1 cm H20/cm height). The more negative pleural liquid pressure is presumed to be the result of an absorptive mechanism which reduced the pleural liquid until the pleural surfaces make contact. We will re-examine these postulates using new techniques. We developed two relatively noninvasive techniques for measureing pleural liquid pressure: the micropipet-servonulling and the rib capsule techniques. Measurement in rabbits and dogs indicate that pleural liquid pressure is not in static equilibrium but show a vertical gradient of less than 1 cmH20/cm. Measurements of pleural liquid thickness by a new method using light microscopy show no contact between the two pleurae. We shall use these techniques to explore the relationship between pleural liquid pressure, pleural liquid thickness and lung height. First, we shall measure by micropuncture the vertical gradient in pleural liquid pressure in the prone and supine dog. Second, we shall compare pleural liquid pressure in the lobar margins and on the diaphragmatic surface with the pressure over the costal surface. Also we shall measure pleural thickness at the fissure by light microscopy. Third, we found that the pleural space thickness measured using light microscopy in 5 species increased with animal size. We will extend these measurements to a larger species, the sheep. Fourth, we will measure by a gamma camera the pleural liquid thickness and the dynamics of pleural liquid. Our results suggest that the dynamics of pleural liquid is important. Recently, we proposed a theory of pleural liquid exchange which includes viscous flow within the pleural space. Pleural liquid exchange is governed by the laws of liquid and solute exchange across the microvasclar barrier. The viscous flow is driven by regional differences in pleural surface pressure and gravity. Pleural liquid pressure equals surface pressure. In the steady state the exchange rate equals the viscous flow which is a funciton of the pleural space thickness. To test our hypothesis, we will measure pleural liquid thickness, microvascular pressure and pleural liquid protein concentration in spontaneously hypertensive rats (SHR) and control normotensive rats (WKY). Elevation in blood pressure should increase flow, increase thickness, and decrease protein concentration.